Transcript Arrhythmias 101

Arrhythmias 101
Fundamentals and what you should
know for the big, bad BOARDS!
The Basics
• SA Node and AV node cells are slow
conductors activated by calcium, thus
blocked by calcium channel blockers
such as verapamil
• Atrium, Bundle of His, and ventricle
cells are fast conducting and activated
by sodium, thus blocked by sodium
channel blockers (class 1 antiarrhythmics) such as quinidine,
lidocaine and propafenone.
4 Mechanisms of Arrhythmia
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reentry (most common)
automaticity
parasystole
triggered activity
Reentry Requires…
Electrical Impulse
Cardiac
Conduction
Tissue
Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
1. 2 distinct pathways that come together at
beginning and end to form a loop.
2. A unidirectional block in one of those pathways.
3. Slow conduction in the unblocked pathway.
Reentry Mechanism
Premature Beat Impulse
Cardiac
Repolarizing Tissue
Conduction
(long refractory period)
Tissue
Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
1. An arrhythmia is triggered by a premature beat
2. The fast conducting pathway is blocked because of its
long refractory period so the beat can only go down the
slow conducting pathway
Reentry Mechanism
Cardiac
Conduction
Tissue
Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
3. The wave of excitation from the premature beat
arrives at the distal end of the fast conducting
pathway, which has now recovered and therefore
travels retrogradely (backwards) up the fast pathway
Reentry Mechanism
Cardiac
Conduction
Tissue
Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
4. On arriving at the top of the fast pathway it finds the
slow pathway has recovered and therefore the wave of
excitation ‘re-enters’ the pathway and continues in a
‘circular’ movement. This creates the re-entry circuit
Reentry Circuits
AV Nodal Reentry
•SVT
Atrial Reentry
• atrial tachycardia SA Node
• atrial fibrillation
• atrial flutter
Atrio-Ventricular
Reentry
• WPW
• SVT
Ventricular Re-entry
• ventricular tachycardia
Reentry Requires…
1. 2 distinct pathways that come together at
beginning and end to form a loop.
2. A unidirectional block in one of those
pathways.
3. Slow conduction in the unblocked pathway.
Large reentry circuits, like a-flutter, involve the
atrium.
Reentry in WPW involves atrium, AV node,
ventricle and accessory pathways.
Automaticity
• Heart cells other than those of the SA node
depolarize faster than SA node cells, and
take control as the cardiac pacemaker.
• Factors that enhance automaticity include:
 SANS,  PANS,  CO2,  O2,  H+,  stretch,
hypokalemia and hypocalcaemia.
Examples: Ectopic atrial tachycardia or
multifocal tachycardia in patients with chronic
lung disease OR ventricular ectopy after MI
Parasystole…
• is a benign type of automaticity
problem that affects only a small region
of atrial or ventricular cells.
• 3% of PVCs
Triggered activity…
• is like a domino effect where the arrhythmia
is due to the preceding beat.
• Delayed after-depolarizations arise during
the resting phase of the last beat and may be
the cause of digitalis-induced arrhythmias.
• Early after-depolarizations arise during the
plateau phase or the repolarization phase of
the last beat and may be the cause of
torsades de pointes (ex. Quinidine induced)
Diagnosis…
What tools to use and when to use
it…
Event Monitors
• Holter monitoring: Document symptomatic
and asymptomatic arrhythmias over 24-48
hours. Can also evaluate treatment
effectiveness in a-fib, pacemaker
effectiveness and identify silent MIs.
• Trans-telephonic event recording: patient
either wears monitor for several days or
attaches it during symptomatic events and an
ECG is recorded and transmitted for
evaluation via telephone. Only 20% are
positive, but still helpful.
Exercise testing
• Symptoms only appear or worsen with
exercise.
• Also used to evaluate medication
effectiveness (esp. flecanide & propafenone)
 You can assess SA node function with exercise testing.
 Mobitz 1 (Wenkebach) is blockage at the AV node, so
catecholamines from exercise actually help!
 Mobitz 2 is blockage at bundle of His, so it worsens as
catecholamines from exercise increase AV node
conduction, thus prognosis is worse.
*PVCs occur in 10% without and 60% of patients
with CAD. *PVCs DO NOT predict severity of
CAD (neither for nor against)!
Signal Averaged ECG
• Used only in people post MI to evaluate risk
for v-fib or v-tach.
• Damage around the infarct is variable, so
this measures late potentials (low-signal,
delayed action potentials) as they pass
through damaged areas.
• Positive predictive value is 25%-50% but
negative predictive value is 90%-95%, thus if
test is negative, patient is at low risk.
Electrophysiologic Testing…
• Catheters are placed in RA, AV node,
Bundle of HIS, right ventricle, and coronary
sinus (to monitor LA and LV).
• Used to evaluate cardiogenic syncope of
unknown origin, symptomatic SVT,
symptomatic WPW, and sustained v-tach.
*Ablative therapy is beneficial in AV node
reentry, WPW, atrial tachycardia, a-flutter,
and some v-tach. Complication is 1%
Bradyarrhythmias
The slow pokes (HR<60)…
Sick Sinus Syndrome
• Conduction problem with no junctional
escape during sinus pause
• Diagnose with ECG or Holter. If inconclusive,
need electrophysiologic testing.
• If asymptomatic, leave alone. If symptomatic,
needs pacemaker.
First Degree AV Block
• Delay at the AV node results in prolonged
PR interval
• PR interval>0.2 sec.
• Leave it alone
Second Degree AV Block
Type 1 (Wenckebach)
•
Increasing delay at AV node until a p wave is not
conducted.
• Often comes post inferior MI with AV node ischemia
• Gradual prolongation of the PR interval before a
skipped QRS. QRS are normal!
• No pacing as long as no bradycardia.
Second Degree AV Block
Type 2
•
Diseased bundle of HIS with BBB.
• Sudden loss of a QRS wave because p
wave was not transmitted beyond AV node.
QRS are abnormal!
• May be precursor to complete heart block
and needs pacing.
Third Degree AV Block
•
Complete heart block where atria and
ventricles beat independently AND atria beat
faster than ventricles.
• Must treat with pacemaker.
LBBB
Left Bundle Branch Block
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Left ventricle gets a delayed impulse
QRS is widened (at least 3 boxes)
V5 and V6 have RR’ (rabbit ears)
Be careful not to miss any hiding q waves!
Pacemaker if syncope occurs
Right Bundle Branch Block
Right Bundle Branch Block
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Right ventricle gets a delayed impulse
QRS is widened (at least 3 boxes)
V1 and V2 have rSR’
Pacemaker if syncope occurs.
Bifascicular Block
• RBBB plus LABB OR RBBB plus LPBB
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QRS is widened (at least 3 boxes)
V5 and V6 have RR’ (rabbit ears)
V1 and V2 have rSR’
Pacemaker if syncope occurs
Tachyarrhythmias
The speed demons…(HR >100)
Tachyarrhythmias
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Supraventricular tachycardia
Atrial fibrillation
Atrial flutter
Ventricular tachycardia
» Monomorphic
» Polymorphic (Torsades de pointe)
• Ventricular fibrillation
Supraventricular Tachycardia
SVT
• Reentrant arrhythmia at AV node that is
spontaneous in onset
• May have neck fullness, hypotension and/or
polyuria due to ANP
• Narrow QRS with tachycardia
• First line is vagal maneuvers
• Second line is adenosine or verapamil
• For chronic SVT, class 1A or 1C or
amiodarone or sotalol work well
• Ablation will cure it too, but we usually do this
only in young patients
Multifocal Atrial Tachycardia
MAT
• Automatic atrial rhythm from various
different foci
• Seen in hypoxia, COPD, atrial stretch
and local metabolic imbalance.
• Three or more types of p waves and a
rate > 100
• Digoxin worsens it, so treat with oxygen
and slow channel blocker like verapamil
or diltiazem.
Wolf Parkinson White
WPW
• Ventricles receive partial signal normally and
partially through accessory pathway
• Symptomatic tachycardia, short PR interval
(<0.12), a delta wave and prolonged QRS
(>0.12)
• Electrophysiologic testing helps to identify
the reentry pathway and location of the
accessory pathway
WPW
 Because WPW has both normal conduction through
the AV node and accessory pathway conduction that
bypasses the AV node, a-fib can happen via the
accessory pathway
 Inhibition of the AV node will end up in worsening the
a-fib because none of the signals are slowed down
by the AV node before hitting the ventricle.
* Do not use any meds that will slow AV node
conduction, ie digoxin, beta-blockers, adenosine or
calcium channel blockers.
* The best choice is procainamide as it slows the
accessory pathway. *If patient becomes
hypotensive, cardiovert immediately!
Atrial Flutter
Atrial Flutter
• Atrial activity of 240-320 with sawtooth
pattern. Usually a 2:1 conduction pattern; if it
is 3:1 or higher, there is AV node damage
• Treatment is to slow AV node conduction with
amiodarone, propafenone or sotalol
• DC cardiovert if <48 hours or unstable
• You can also ablate the reentry pathway
within the atrium between the tricuspid and
the IVC.
Atrial Fibrillation
A-Fib
• Can be due to HTN, cardiomyopathy,
valvular heart desease, sick sinus,
WPW, thyrotoxicosis or ETOH
• Therapy is either rate control via
slowing AV node conduction with stroke
prophylaxis or rhythm control
Rate control
 Beta-blockers
 Continuation after CABG may prevent a-fib
 Good for hyperthyroid or post-MI patients with a-fib
 Carvedilol decreases mortality in patients with CHF
 Esmolol is good for acute management
 Digoxin actually increases vagal tone, thus
indirectly slowing AV node conduction. But it is
used essentially only in patients with LV
dysfunction because it’s inotropic.
Rate control
 Calcium Channel Blockers
 Nondihydropyridines (verapamil or dilitiazem)
block AV node conduction but also have negative
inotropy, so don’t use in CHF.
 Dihydropyridines (nifedipine, amlodipine,
felodipine) have no effect on AV node conduction
 Adenosine is too short acting to be of any
use in a-fib
 Last choice is AV node ablation and
permanent pacing
Rhythm control
 Rhythm control does not decrease
thromboembolic risk and may be
proarrhythmic
 Class 1A (quinidine, procainamide, disopyramide) slows
conduction through HIS can cause torsades de pointes
during conversion. They also enhance AV node
conduction, so they should be used only after rate is
controlled
 Class 1B (lidocaine, meilitine, tocainide) are useless for
a-fib
 Class 1C (propafenone, and flecainide) slow conduction
through HIS are good first choice.
• Amiodarone is good if patient is post-MI or
has systolic dysfunction.
Cardioversion for A-Fib
• Cardiovert if symptomatic
• Patients with a-fib for more than 2 days
should be receive 3 weeks of
anticoagulation before electrical
cardioversion.
• Give coumadin for 4 weeks after
cardioversion
Anticoagulation Rules for
A-Fib
 Everybody who has rheumatic heart disease
should be anticoagulated
 If <65 yo and with h/o DM, HTN, CHF, CVA,
prosthetic valves, thyrotoxicosis, LV
dysfunction or LA enlargement, then give
coumadin
 If no risk factors, do nothing.
 65-75 yo with any of above risk factors, give
coumadin; if no additional risk factors, give
coumadin or aspirin
 >75 yo give coumadin but keep INR 2-2.5
due to increased risk of bleed
Ventricular Tachycardia
Ventricular Tachycardia
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Impulse is initiated from the ventricle itself
Wide QRS, Rate is 140-250
If unstable DC cardiovert
If not, IV Amiodarone and/or DCCV
Consider procainamide
• Nonsustained ventricular tachycardia needs no
treatment
Torsades de Pointes
• “Twisting of the points” is usually caused by
medication (quinidine, disopyramide, sotalol, TCA),
hypokalemia or bradycardia especially after MI
• Has prolonged QT interval
• Acute: Remove offending medication. Shorten the
QT interval with magnesium, lidocaine, isoproterenol,
or temporary overdrive pacing
• Chronic: may need pacemaker/ICD, amiodarone,
beta-blockers
Ventricular Fibrillation
• Most common in acute MI, also drug
overdose, anesthesia, hypothermia & electric
shock can precipitate
• Absence of ventricular complexes
• Usually terminal event
• Use Amiodarone if refractory to DCCV.
Treatment
Here comes the fun part!
Classification of Anti-arrhythmics
Cla ss
1A
Actio n
Fa st so d ium chan ne l b lo cke r va ries
d e p o la riza tio n a n d a ction p o te n tial
d u ra tio n
Exa mp le s
Q u inidine ,
p ro ca ina mid e,
d iso p y ra mid e
1B
Lid o ca ine,
Mex ile tine
1C
b eta-b locke rs SA no d e & AV no d e
co nd uctio n
P ro lo ng a ctio n p o ten tia l b y b locking
K+ c ha nne ls
Fle ca inide,
P ro p afen o ne
P ro p ra no lo l,
me to p ro lol
Amio d a ro ne,
so ta lo l
cal cium cha nne l b lo cke rs AV no d e
co nd uctio n
Ve ra p a mil,
d ilitia z e m
2
3
4
Sid e Ef fe cts
Cla ss: na use a , vo miting
Q u inidine : h e mo ly tic
a ne mia, thro mb o cyto p e n ia ,
tinnitus
P ro cai n a mid e : lup us
Lid o ca ine: d izz ines s,
co nfu sio n, seizure s, co ma
Mex ile tine : tre mo r, a taxia,
ras h
Fle ca inide: p ro -a rrhy thmia ,
na usea , d iz zy ne ss
Cla ss: CHF, b ro ncho sp a sm,
b ra d yca rd ia , h yp o ten sion
Amio d a ro ne: he p a titis,
p u lmo na ry fi b ro sis, thyro id
d iso rd e rs, p e riph e ra l
neu ro p a thy
So talo l: b ro ncho spa sm
Cla ss: AV b lo ck,
hyp o te nsio n, b ra d ycar d ia,
co nstipa tio n
Where did you say you
worked?
Locat ion of A ctivity
AV No de
AV No de , Accessory Pa thway, Bundle of
HIS, ventricle
Atria l, Ven tricular, Acce ssory Pa thwa y,
Bund le of HI S
Anti-arrh ythmic
Aden osine, Ca lcium chann el blockers, Bb locker s, Digoxin
Propaf enone, Amioda ro ne, Soto lol
Q uinidine , Pro ca ina mide , Lido ca ine,
Disopy ram ide, F le can ide, Ibu tilide,
Bret ylium, Dofet ilide
When in
doubt…Amiodarone
Amiodarone
IV
SVT
VT
Atrial Fib or flutter
Amiodarone.
Modes of action.
• Mainly class III action on the outgoing
K+ channels.
• Class Ib action on the Na+ channels.
• Non competitive alpha antagonism
(class III)
Magnesium indications.
• 1. Torsades de point from any reason.
• 2. Arrhythmias in a patient with known
hypomagnesaemia.
• 3. Consider its use in acute ischaemia to
prevent early ventricular arrhythmias.
• 4. Digoxin induced arrhythmias.
Who gets a pacemaker?
 Syncope, presyncope or exercise intolerance
that can be attributed to bradycardia
 Symptomatic 2nd or 3rd degree AV block
 Congenital 3rd degree AV block with wide QRS
 Advanced AV block after cardiac surgery
 Recurrent type 2 2nd degree AV block after MI
 3rd degree AV block with wide QRS or BBB.
QUESTIONS